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5 results on '"SOFA, Sequential organ failure assessment score"'

1. MMP-2 and MMP-9 levels in plasma are altered and associated with mortality in COVID-19 patients

Author

Bruno C. Petroski-Moraes, Katarzyna Polonis, Denise Ferro, Ligia Borges Campos, Paulo Roberto Barbosa Evora, Carlos Alexandre Curylofo Corsi, Ariel Emiliano Souza do Couto, Rodrigo de Carvalho Santana, Christiane Becari, Maria Auxiliadora-Martins, Maria J. Garbellini-Diab, Olindo Assis Martins-Filho, Maria Cecília Jordani, Lourenço Sbragia, Mayra Gonçalves Menegueti, Edwaldo Edner Joviliano, Carolina D`Avila-Mesquita, Fabíola Mestriner, Maurício Serra Ribeiro, Daniel M.S. Couto, Tauana F. Vasconcelos, and Jessyca Michelon-Barbosa

Subjects
Male, ACEi, angiotensin-converting enzyme inhibitors, Gastroenterology, Severity of Illness Index, Body Mass Index, SOFA, sequential organ failure assessment score, SARS-COV2 infection, Risk Factors, Hospital Mortality, ARB, angiotensin receptor blockers, MMP-2, Acute kidney injury, Age Factors, General Medicine, Middle Aged, MMP-2, Matrix Metalloproteinase 2, Prognosis, Metalloproteinases, Pathophysiology, Intensive Care Units, Matrix Metalloproteinase 9, COVID-19, Coronavirus Disease 2019, Ang, angiotensin, Hypertension, ÍNDICE DE GRAVIDADE DA DOENÇA, Matrix Metalloproteinase 2, Female, MMP-9, Brazil, COVID-19 pathophysiology, medicine.medical_specialty, ACE, angiotensin-converting enzyme, RM1-950, MMP-9, Matrix Metalloproteinase 9, ACE2, angiotensin-converting enzyme 2, Article, iRAAs, inhibitors of the renin-angiotensin system, Predictive Value of Tests, Diabetes mellitus, Internal medicine, Severity of illness, medicine, Humans, Mortality, Survival analysis, Pharmacology, AKI, Acute Kidney Injury, SAPS3, Simplified Acute Physiology Score III, business.industry, SARS-CoV-2, COVID-19, RAS, renin-angiotensin system, medicine.disease, Obesity, Comorbidity, MMPs, metalloproteinases, SARS-CoV-2, Severe Acute Respiratory Syndrome Coronavirus 2, Therapeutics. Pharmacology, business, Body mass index
Abstract

Respiratory symptoms are one of COVID-19 manifestations, and the metalloproteinases (MMPs) have essential roles in the lung physiology. We sought to characterize the plasmatic levels of matrix metalloproteinase-2 and 9 (MMP-2 and MMP-9) in patients with severe COVID-19 and to investigate an association between plasma MMP-2 and MMP-9 levels and clinical outcomes and mortality. MMP-2 and MMP-9 levels in plasma from patients with COVID-19 treated in the ICU (COVID-19 group) and Control patients were measured with the zymography. The study groups were matched for age, sex, hypertension, diabetes, BMI, and obesity profile. MMP-2 levels were lower and MMP-9 levels were higher in a COVID-19 group (p, Graphical Abstract ga1

Published
2021

2. Cytokine storm in the pathophysiology of COVID-19: Possible functional disturbances of miRNAs

Author

Seyed Shahabeddin Mortazavi-Jahromi, Abbas Mirshafiey, and Mona Aslani

Subjects
RhoB, Ras homolog gene family member B, M-CSF, Macrophage CSF, PPP2CA, Protein phosphatase 2 catalytic subunit alpha, RNA pol, RNA polymerase, medicine.medical_treatment, IRF, IFN regulatory factor, v-miRNA, Viral miRNA, DCs, Dendritic cells, MyD88, Myeloid differentiation factor 88, ISGs, IFN-stimulated genes, TLRs, Toll-like receptors, AT1R, Ang II receptor type 1, KCNQ1OT1, KCNQ1 overlapping transcript 1, CYLD, Cylindromatosis, IFNs-I, Type I IFNs, TNF-α, Tumor necrosis factor alpha, cPLA2, Cytoplasmic phospholipase A2, LPS, Lipopolysaccharide, Th cells, T helper cells, LPLs, Lysophospholipids, NLRP3, NOD-, LRR- and pyrin domain-containing protein 3, siRNAs, Small interfering RNAs, CNS, Central nervous system, pri-miRNAs, Primary miRNAs, MDA5, Melanoma differentiation-associated protein 5, ERK, Extracellular signal-regulated kinase, MERS-CoV, Middle East respiratory syndrome coronavirus, BBB, Blood-brain barrier, OxPLs, Oxidized phospholipids, MODS, Multiple organ dysfunction syndrome, mPGES-1, Microsomal prostaglandin E synthase-1, RNAi, RNA interference, ADAM17, A disintegrin and metalloproteinase 17, AGO, Argonaute, CRISPR, Cas13 family of clustered regularly interspaced short palindromic repeats, DAMPs, Damage-associated molecular patterns, circRNAs, Circular RNAs, CD, Cluster of differentiation, JAK, Janus kinase, TNFR, TNF receptor, Cytokine Release Syndrome, TRIM27, Tripartite motif-containing protein 27, gp130, Glycoprotein 130, MMP, Matrix metalloproteinase, 2019-nCoV, 2019 novel coronavirus, CCL, C-C motif chemokine ligand, SOCS3, Suppressor of cytokine signaling 3, Immunology, COX, Cyclooxygenase, Sry, Sex-determining region Y, Article, S protein, Spike protein, microRNA, Humans, K, Lysine, CSF, Colony-stimulating factor, RGMB-AS1, RGMB antisense RNA 1, TIMP-I, Tissue inhibitors of matrix metalloproteinases-I, S100A9, S100 calcium-binding protein A9, Pharmacology, SARS-CoV-2, Severe acute respiratory syndrome coronavirus 2, NOXs, Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, CHD, Coronary heart disease, STAT, Signal transducer and activator of transcription, Virus Internalization, medicine.disease, Viral replication, NF-κB, Nuclear factor kappa-light-chain-enhancer of activated B cells, miRNAs-based therapy, TBK1, TANK-binding kinase 1, ORF, Open reading frame, SOFA, Sequential organ failure assessment score, lncRNAs, Long non-coding RNAs, CatB/L, Cathepsin B/L, sIL-6R, Soluble IL-6R, ROS, Reactive oxygen species, EAE, Experimental autoimmune encephalomyelitis, RBCs, Red blood cells, MAPK, Mitogen-activated protein kinase, PBMCs, Peripheral blood mononuclear cells, N protein, Nucleocapsid protein, Ig, Immunoglobulin, Cytokine storm, Bioinformatics, Virus Replication, 3'-UTR, 3'-untranslated region, H3, Histone 3, AGEs, Advanced glycation end products, Renin-Angiotensin System, XPO5, Exportin-5, G-CSF, Granulocyte CSF, CXCL, C-X-C motif chemokine ligand, DIC, Disseminated intravascular coagulation, Immunology and Allergy, IL, Interleukin, PG, Prostaglandin, RAS, Renin-Angiotensin system, Amp, Amplifier, MCs, Mast cells, COVID-19, Coronavirus disease 2019, HSP, Heat shock protein, AA, Arachidonic acid, ASOs, Antisense oligonucleotides, IFN, Interferon, mRNA, Messenger RNA, ICU, Intensive care unit, Cytokine, RAGE, Receptor for advanced glycation end products, mIL-6R, Membrane IL-6 receptor, FOXO3, Forkhead box O3, miRNAs, LTs, Leukotrienes, miRISC, MicroRNA-induced silencing complex, IκB-ζ, Inhibitor of nuclear factor kappa B zeta, Signal transduction, me3, Trimethylation, M protein, Membrane protein, APJ, Apelin receptor, AP-1, Activator protein 1, TMPRSS2, Transmembrane serine protease 2, PRR, Pattern recognition receptor, GM-CSF, Granulocyte-macrophage CSF, RIG-I, Retinoic acid-inducible gene I, E protein, Envelope protein, Biology, hsa, Homo sapiens, TXs, Thromboxanes, LOXs, Lipoxygenases, Virus, ER, Endoplasmic reticulum, ARDS, Acute respiratory distress syndrome, Gene regulators, medicine, me2, Dimethylation, Animals, PKCα, Protein kinase C alpha, pre-miRNAs, Precursor miRNAs, DMVs, Double membrane vesicles, ceRNAs, Competing endogenous RNAs, nsp, Non-structural protein, Competing endogenous RNA, SARS-CoV-2, ALI, Acute lung injury, PaO2/FiO2, Pressure of arterial oxygen to fractional inspired oxygen concentration, COVID-19, ACE, Angiotensin-converting enzyme, ANRIL, Antisense noncoding RNA in the INK4 locus, miRNAs, MicroRNAs, MEG3, Maternally expressed gene 3, Review article, MicroRNAs, DMD, Dense matted deposits, TAB, Transforming growth factor β-activated kinase-1 (TAK1)-binding protein, HMGB1, High mobility group box protein 1, Ang, Angiotensin
Abstract

SARS-CoV-2, as the causative agent of COVID-19, is an enveloped positives-sense single-stranded RNA virus that belongs to the Beta-CoVs sub-family. A sophisticated hyper-inflammatory reaction named cytokine storm is occurred in patients with severe/critical COVID-19, following an imbalance in immune-inflammatory processes and inhibition of antiviral responses by SARS-CoV-2, which leads to pulmonary failure, ARDS, and death. The miRNAs are small non-coding RNAs with an average length of 22 nucleotides which play various roles as one of the main modulators of genes expression and maintenance of immune system homeostasis. Recent evidence has shown that Homo sapiens (hsa)-miRNAs have the potential to work in three pivotal areas including targeting the virus genome, regulating the inflammatory signaling pathways, and reinforcing the production/signaling of IFNs-I. However, it seems that several SARS-CoV-2-induced interfering agents such as viral (v)-miRNAs, cytokine content, competing endogenous RNAs (ceRNAs), etc. preclude efficient function of hsa-miRNAs in severe/critical COVID-19. This subsequently leads to increased virus replication, intense inflammatory processes, and secondary complications development. In this review article, we provide an overview of hsa-miRNAs roles in viral genome targeting, inflammatory pathways modulation, and IFNs responses amplification in severe/critical COVID-19 accompanied by probable interventional factors and their function. Identification and monitoring of these interventional elements can help us in designing the miRNAs-based therapy for the reduction of complications/mortality rate in patients with severe/critical forms of the disease.

Published
2021

3. Therapeutic versus prophylactic anticoagulation for severe COVID-19: A randomized phase II clinical trial (HESACOVID)

Author

Maísa Cabetti Salvetti, Antonio Pazin-Filho, Anna Cristina Bertoldi Lemos, Lucas Barbosa Agra, Douglas Alexandre do Espírito Santo, Renato Noffs Gilio, and Carlos Henrique Miranda

Subjects
Male, Time Factors, BMI, body mass index, medicine.medical_treatment, Letter to the Editors-in-Chief, PEEP, positive end-expiratory pressure, 030204 cardiovascular system & hematology, RT-PCR, reverse transcriptase-polymerase chain reaction, SOFA, sequential organ failure assessment score, ULN, upper limit of normal, Mechanical ventilation, 0302 clinical medicine, FiO2, fraction of inspired oxygen, Coagulopathy, Interquartile range, SIC, sepsis-induced coagulopathy score, Fraction of inspired oxygen, CrCl, creatinine clearance, Thrombophilia, CKD-EPI, Chronic Kidney Disease Epidemiology Collaboration, DIC, disseminated intravascular coagulation, Lung, COVID-19, Coronavirus disease 2019, Anticoagulant, Hazard ratio, Hematology, Middle Aged, ICU, intensive care unit, Treatment Outcome, 030220 oncology & carcinogenesis, Anesthesia, Female, PaO2, partial pressure of arterial oxygen, Brazil, Adult, Randomization, medicine.drug_class, aPTT, activated partial thromboplastin time, Drug Administration Schedule, 03 medical and health sciences, Full Length Article, medicine, Humans, SAPS3, simplified acute physiology score 3, UFH, unfractionated heparin, Enoxaparin, ARDS, acute respiratory distress syndrome, IQR, interquartile range, Aged, business.industry, Pulmonary Gas Exchange, Anticoagulants, COVID-19, Thrombosis, Respiration, Artificial, Confidence interval, LMWH, low molecular weight heparin, COVID-19 Drug Treatment, CI, confidence interval, Clinical trial, D-dimer, Anticoagulant treatment, business
Abstract

Introduction Coronavirus disease 2019 (COVID-19) causes a hypercoagulable state. Several autopsy studies have found microthrombi in pulmonary circulation. Methods In this randomized, open-label, phase II study, we randomized COVID-19 patients requiring mechanical ventilation to receive either therapeutic enoxaparin or the standard anticoagulant thromboprophylaxis. We evaluated the gas exchange over time through the ratio of partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FiO2) at baseline, 7, and 14 days after randomization, the time until successful liberation from mechanical ventilation, and the ventilator-free days. Results Ten patients were assigned to the therapeutic enoxaparin and ten patients to prophylactic anticoagulation. There was a statistically significant increase in the PaO2/FiO2 ratio over time in the therapeutic group (163 [95% confidence interval – CI 133–193] at baseline, 209 [95% CI 171–247] after 7 days, and 261 [95% CI 230–293] after 14 days), p = 0.0004. In contrast, we did not observe this improvement over time in the prophylactic group (184 [95% CI 146–222] at baseline, 168 [95% CI 142–195] after 7 days, and 195 [95% CI 128–262] after 14 days), p = 0.487. Patients of the therapeutic group had a higher ratio of successful liberation from mechanical ventilation (hazard ratio: 4.0 [95% CI 1.035–15.053]), p = 0.031 and more ventilator-free days (15 days [interquartile range IQR 6–16] versus 0 days [IQR 0–11]), p = 0.028 when compared to the prophylactic group. Conclusion Therapeutic enoxaparin improves gas exchange and decreases the need for mechanical ventilation in severe COVID–19. Trial registration REBEC RBR-949z6v., Highlights • COVID-19 is associated with microthrombi in pulmonary circulation. • We randomized severe COVID-19 patients to receive either therapeutic enoxaparin or the standard thromboprophylaxis. • Therapeutic enoxaparin resulted in improved gas exchange over time. • Larger clinical trial is urgently needed to evaluate the anticoagulant therapy in severe COVID-19.

Published
2020
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4. Complications of invasive mechanical ventilation in critically Ill Covid-19 patients - A narrative review.

Author

Khan W, Safi A, Muneeb M, Mooghal M, Aftab A, and Ahmed J

Abstract

Critically ill COVID-19 patients have to undergo positive pressure ventilation, a non-physiological and invasive intervention that can be lifesaving in severe ARDS. Similar to any other intervention, it has its pros and cons. Despite following Lung Protective Ventilation (LPV), some of the complications are frequently reported in these critically ill patients and significantly impact overall mortality. The complications related to invasive mechanical ventilation (IMV) in critically ill COVID-19 patients can be broadly divided into pulmonary and non-pulmonary. Among pulmonary complications, the most frequent is ventilator-associated pneumonia. Others are barotrauma, including subcutaneous emphysema, pneumomediastinum, pneumothorax, bullous lesions, cardiopulmonary effects of right ventricular dysfunction, and pulmonary complications mimicking cardiac failure, including pulmonary edema. Tracheal complications, including full-thickness tracheal lesions (FTTLs) and tracheoesophageal fistulas (TEFs) are serious but rare complications. Non-Pulmonary complications include neurological, nephrological, ocular, and oral complications., Competing Interests: We do not have any conflicts of interest., (© 2022 The Author(s).)

Published
2022
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5. Role of Transient Elastography (Fibroscan) in Differentiating Severe Acute Hepatitis and Acute on Chronic Liver Failure.

Author

Sharma P, Bansal R, Matin A, Tyagi P, Bansal N, Singla V, Kumar A, and Arora A

Abstract

Introduction: It is difficult to differentiate acute severe hepatitis (AH) with acute on chronic liver failure (ACLF). Aim was to study the role of transient elastography (Fibroscan) in identifying the patients with AH and ACLF., Materials and Methods: Consecutive patients of severe AH or ACLF presented within two weeks of jaundice were enrolled. LSM and liver function tests were done at admission, week 1, 4 and at 6 months. Diagnosis of ACLF was based on documenting cirrhotic morphology on imaging and/or liver biopsy and follow-up of these patients for six months. Similarly, AH patients were diagnosed based on serology, no features of cirrhosis on imaging and follow-up of these patients for 6 months documenting reversal of liver stiffness measurement (LSM) to normal., Results: 104 patients were included in the final analysis (AH, n = 59, ACLF, n = 45). Out of 59 patients in severe AH group, etiology of acute hepatitis included hepatitis A (HAV, n = 22), hepatitis E (HEV, n = 21), hepatitis B (HBV, n = 4), indeterminate (n = 8) and drug induced liver injury (n = 4). Similarly for ACLF, the causes of chronic liver disease were alcohol (n = 26), hepatitis B (n = 7), hepatitis C (n = 2) and cryptogenic (n = 10). Patients with ACLF were significantly older, had low hemoglobin, low albumin, high bilirubin and lower transaminases level compared to severe AH at admission. LSM was higher in patients with ACLF compared to severe AH (61 ± 18 kPa vs 15 ± 6.4 kPa, P = 0.001) at admission. On multivariate analysis of noninvasive tests only LSM was found to differentiate AH with ACLF significantly. When we took a cutoff of 26 kPa the sensitivity and specificity of diagnosis of ACLF were 96% and 93%, respectively, with area under the curve was 0.98 (0.95-1.005), P = 0.001., Conclusion: LSM could differentiate patients with severe AH and ACLF at admission.

Published
2015
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